Immune mechanisms are responsible for hematopoietic failure in most cases of acquired aplastic anemia (AA), a disease characterized by hypocellular bone marrow and pancytopenia. In aplastic anemia, much experimental data points toward an immune-mediated pathophysiology of destruction of hematopoietic progenitor and stem cells. Clinically, immunosuppressive therapies, usually anti-thymocyte globulin (ATG) and cyclosporine (CsA), have been shown to be effective in a large proportion of patients with severe AA. However, at 2 years after initial treatment as many as 35% of patients with initially good response and normal blood counts relapse and require repeated cycles of intense immunosuppression and/or chronic immunosuppressive regimens. Although relapse in previously immunosuppression-responsive patients has a generally good prognosis, there is an increased risk of complications and treatment-related toxicities. The outlook of patients who fail to respond to repeated intensive immunosuppression is poor. While it is likely that some of the treatment failures occurring with conventional immunosuppressive regimens (both at presentation and in relapsed patients) may be due to inability to suppress the autoimmune process leading to the bone marrow failure, more intense therapies such as cyclophosphamide have a high complication rate due to prolonged and dose-related myelosuppression. In this protocol, we propose that patients with severe AA who show a good response to the initial round of immunosuppression undergo stem cell mobilization, collection, and cryopreservation.